A sequential study of experimental infection of pigs with porcine circovirus and porcine parvovirus: immunostaining of cryostat sections and virus isolation

The sequential tissue distribution of virus was investigated using virus isolation and immunofluorescence tests in 1-day-old piglets inoculated with porcine circovirus 2 (PCV2) and/or porcine parvovirus (PPV). Enlarged mesenteric lymph nodes were seen in the pig inoculated with PCV2 alone and killed at 26 days post-inoculation (PI). One of the pigs inoculated with PCV2 and PPV and killed at 21 days PI had an enlarged liver. The pig killed at 26 days PI in this group had enlarged liver, kidneys and heart. Histopathological changes were seen in lymphoid tissues of the pigs inoculated with PCV2 alone and killed at 14 and 26 days PI. Similar, but more severe, lesions were observed in the pigs infected with PCV2 and PPV and killed from 10 days PI onwards. Histological lesions of nephritis, pneumonia and hepatitis were also apparent in these animals. Mild nephritis was also seen in the pigs infected with PPV alone and killed at 14 and 26 days PI. Moderate amounts of PPV antigen were detected in tissues from the pigs inoculated with PPV alone and killed at 14 days PI. Low levels of PCV antigen were detected, mainly in lymphoid tissues, in the pigs inoculated with PCV alone and killed at 14 days PI. Low to moderate amounts of PCV antigen were detected in a wider range of tissues in the pig in this group killed at 26 days PI. In the pigs inoculated with both viruses, PPV antigen was detected in tissues of pigs killed from 3 to 26 days PI with maximal amounts detected between 6 and 14 days PI. PCV2 antigen was detected in low to moderate amounts in the tissues of pigs killed at 14 days PI. Large amounts of PCV2 antigen were detected in most of the tissues from pigs in this group killed between 17 and 26 days PI. Virus isolation results for PCV2 generally correlated well with the results for immunofluorescent staining. PPV was isolated from almost all tissues from pigs inoculated with PCV2 and PPV, a much higher incidence of positive tissues than observed for immunofluorescent staining.     

Pathogenicity of a skin isolate of porcine parvovirus in swine fetuses

The pathogenic properties of a skin isolate of porcine parvovirus (PPV), designated Kresse isolate, were compared with NADL-8 isolate, a prototype isolate of PPV, by in utero inoculation of mid-term and late-term gestation swine fetuses. Fetuses from pregnant sows of mid-gestation were inoculated with either NADL-8 or Kresse virus. Both isolates were highly pathogenic to mid-gestation fetuses. In contrast, dramatic differences in pathogenicity between these 2 isolates were observed in fetuses inoculated late in gestation. Such fetuses from each of 4 sows were inoculated with NADL-8 or Kresse virus isolate and sacrificed at 10, 18, 21, or 23 days postinoculation (PI). NADL-8-inoculated fetuses were grossly normal. The pathogenic effects of Kresse isolate were evident by gross pathology in fetuses collected at 18, 21, and 23 days PI, but not at 10 days PI. Hemagglutination (HA) and fluorescent antibody (FA) methods were used to identify virus in various tissues of late-gestation fetuses collected at 10 and 21 days PI. At 10 days PI, HA antigens were detected only in livers of NADL-8-inoculated fetuses, but in all tissues examined of Kresse-inoculated fetuses, including the brain. PPV specific fluorescence was demonstrated in tissues of fetuses inoculated with NADL-8 and Kresse virus. The major difference was that virus antigen was found in the brains of fetuses inoculated with Kresse virus, but not in NADL-8 infected fetuses. At 21 days PI, HA antigen was not detected in any of the tissues of fetuses inoculated with NADL-8 virus, with PPV specific fluorescence by FA being found only in the kidney. However, fetuses inoculated with Kresse virus displayed HA antigen in liver and PPV-specific fluorescence in all tissues tested including the brain. Both isolates induced similar antibody responses, 1:128 to 1:256 at 10 days and 1:512 to 1:1024 at 21 days PI. In addition, immunoglobulin G (IgG) deposits were demonstrated in kidneys and skin of fetuses inoculated with Kresse virus and IgM in brain, but not in tissues from fetuses inoculated with NADL-8 virus.     

Experimental production of congenital persistent swine fever infections: II. Effect on functions of the immune system

Twelve pregnant sows were infected at various stages of gestation with a low-virulent field strain of swine fever (SF) virus. The sows developed neutralizing antibody in serum, colostrum and milk.Only one pig had antibody to SF virus at birth. Twenty-three congenitally infected pigs developed a persistent viraemia. In the plasma samples of these pigs, neither antibodies nor virus-antibody complexes were detected after the disappearance of maternal antibodies.The persistently infected pigs showed a normal antibody response against sheep red blood cells, except in the terminal stage of disease. These observations indicate immunological tolerance to SF virus in these pigs. Immunological tolerance was also induced in pigs which had been infected in utero after the onset of immune competence.The lymphocyte response to phytohaemagglutinin seemed to be slightly depressed in the persistently infected pigs, whereas the response to pokeweed mitogen was comparable with that of control pigs.A clear, cell-mediated immune response to SF virus could not be demonstrated by the lymphocyte stimulation test.Three pigs that were born uninfected did not produce neutralizing antibody following natural exposure from in-contacts, whereas the littermates did. These pigs appeared to be sensitized when challenged with virulent SF virus.     

Pathogenesis of porcine reproductive and respiratory syndrome virus infection in mid-gestation sows and fetuses.

Two experiments were undertaken to evaluate whether porcine reproductive and respiratory syndrome (PRRS) virus was able to cross the placenta and infect midgestation fetuses following intranasal inoculation of sows and whether PRRS virus directly infected fetuses following in utero inoculation. In experiment 1, eight sows between 45 and 50 days of gestation were intranasally inoculated with PRRS virus (ATCC VR-2332), and four control sows were inoculated with uninfected cell culture lysate. Virus inoculated sows were viremic on postinoculation (PI) days 1, 3, 5, 7 and 9, shed virus in their feces and nasal secretions, and became leukopenic. Sixty-nine of 71 fetuses from principal sows euthanized on PI day 7, 14 or 21 were alive at necropsy and no virus was isolated from any of the fetuses. Two principal sows that farrowed 65 and 67 days PI delivered 25 live piglets and three stillborn fetuses. The PRRS virus was isolated from two live piglets in one litter. In experiment 2, laparotomies were performed on five sows between 40 and 45 days of gestation and fetuses were inoculated in utero with either PRRS virus alone, PRRS virus plus a swine serum containing PRRS antibodies, or uninfected cell culture lysate. Three sows were euthanized on PI day 4 and two sows on PI day 11. Viral replication occurred in fetuses inoculated with virus alone and was enhanced in fetuses inoculated with virus plus antibody. No virus was isolated from control fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of an inactivated virus vaccine for prevention of porcine parvovirus-induced reproductive failure.

Gilts vaccinated IM either once (4 gilts) or twice (2 gilts) with an acetylethyleneimine-inactivated porcine parvovirus (PPV) vaccine before they were bred were subsequently exposed intranasally and orally to virulent PPV at about the 40th day of gestation (from 37 to 43 days). At 2 weeks after vaccination, all had hemagglutination-inhibiting (HI) titers for PPV (from 20 to 80) which decreased by the time the immunity was challenged with virulent virus (from 10 to 40), but increased thereafter (from 160 to 1,280). Titers of singly and doubly vaccinated gilts were similar throughout the experiment. The gilts were killed at about the 84th day of gestation (from 80 to 87 days), and their litters were examined. Litters were comprised of 68 live fetuses and 1 dead fetus (7 to 14 fetuses/litter). Neither viral antigen, PPV, nor homologous HI antibody was found in any of the fetuses. In addition, 4 gilts were kept in contact with the vaccinated gilts and were treated similarly except for vaccination. These 4 gilts remained free of HI antibody until after they were exposed to virulent PPV during gestation. At the time the gilts were killed the titers were 1,280 to 2,560. Their litters were comprised of 11 live fetuses and 26 dead fetuses (8 to 11 fetuses/litter). Virus was isolated from fetuses of all litters. Viral antigen was found in 24 of the dead fetuses and 10 of the live fetuses. All infected live fetuses also had HI antibody for PPV. The 2 boars used to breed vaccinated and nonvaccinated gilts (usually each gilt was bred to each of the 2 boars), but not exposed to virulent PPV, remained free of HI antibody for PPV.     

Detection of antibodies against porcine parvovirus nonstructural protein NS1 may distinguish between vaccinated and infected pigs

The humoral antibody response against the nonstructural protein NS1 and the structural protein VP2 of porcine parvovirus (PPV) was evaluated by immuno-peroxidase test (IPT) and enzyme linked immuno sorbent assay (ELISA) using recombinant PPV antigens. The coding sequence for NS1 and VP2 was inserted into the baculovirus Autographa californica nuclear polyhedrosis virus (AcNPV) genome resulting in two recombinant baculoviruses AcNPV-NS1 and AcNPV-VP2, respectively. Sf9 cells (Spodoptora frugidiperda) inoculated with AcNPV-NS1 producing recombinant nonstructural protein (rNS1) and AcNPV-VP2 producing recombinant virion protein (rVP2) were used in IPT and ELISA to analyse serum antibodies. Pigs vaccinated with an inactivated whole virus vaccine and experimentally infected pigs were studied. Significant titers against rVP2 were obtained in both vaccinated and infected pigs. Specific antibodies against rNS1 could only be detected in infected pigs and NS1 may in this way allow the specific detection of infected animals. Analysis of serum samples collected up to 18 days post infection (p.i.) from four pigs experimentally infected with PPV showed that antibodies against rNS1 and rVP2 could in all cases be detected on day 9 p.i. Two individual pigs were inoculated twice with PPV and the antibody response was followed 89 days after second inoculation. Serum antibodies against borth rVP2 and rNS1 could be detected for this period of time.     

Use of an inactivated vaccine for prevention of parvovirus-induced reproductive failure in gilts

Gilts from dams that had been inoculated with inactivated porcine parvovirus (PPV) vaccine before breeding became seronegative to PPV by 26 weeks of age. Vaccination of these gilts with inactivated PPV vaccine at 32 weeks of age resulted in an antibody response that peaked at about 2 weeks after vaccination, with -log10 mean hemagglutination inhibiting (HI) antibody titers of less than 2. In the first-year group (82 gilts), HI titers gradually decreased, 20% of the gilts being seronegative by 6 to 7 weeks after vaccination and 75% being seronegative by 16 weeks after vaccination. In the second-year group, 93 gilts were infected naturally by a field strain of PPV at about 11 weeks after single vaccination with inactivated PPV. Additionally, in the second year, 20 vaccinated and 6 nonvaccinated gilts were immune-challenged with virulent PPV at 10 to 12 weeks after vaccination. Neither field nor challenge PPV infection of vaccinated pregnant gilts caused reproductive failure, even though some of the gilts became seronegative for PPV before challenge. Our findings suggest that single vaccination of gilts with inactivated PPV vaccine should give adequate protection from PPV-induced reproductive failure, even though serum HI titers decrease to an undetectable level shortly before PPV infection.     

In utero transmission of bovine leukemia virus

In an initial study, 18 calves born to cows persistently infected with bovine leukemia virus (BLV) were tested for infective virus and antibodies at birth, and no infected or seropositive animals were found. Four of these calves were maintained in quarters where infected animals were housed, and 3 of the 4 subsequently became infected. These were probably contact infections acquired during, or at some time after, birth. The remaining 14 calves were kept in isolation pens in a building housing no infected cattle. None of this group was found to be BLV infected during 1 year of observation. In further studies, 15 pregnant cows inoculated with BLV became infected. One abortion, considered to be unrelated to the BLV inoculation, occurred 38 days later. The remaining 14 cows gave birth to 1 dead and 14 live calves. The dead calf and its live twin were seropositive for BLV at birth, indicating that they had been infected in utero. The remaining 13 calves were negative for BLV antibodies at birth and remained so during 1 year of observation.     

A longitudinal study of rotavirus antibody titers in swine in a closed specific pathogen-free herd.

In a newly established closed specific pathogen-free (SPF) swine herd, gilt/sow suckling and weaned pig rotavirus specific antibody titers were followed for three lactations by enzyme-linked immunosorbent assay (ELISA) to gain insight into the dynamics of herd antibody titers to group A rotavirus. Among gilts/sows, serum antirotavirus IgG titers increased during each lactation with a subsequent drop in titer between farrowings. Serum antirotavirus IgM titers declined during each lactation and with subsequent parity. Serum antirotavirus IgA titers remained constant during lactations and among parities. In colostrum and milk, antirotavirus IgA antibody was abundant. Differences in titer were not noticed between gilts and second litter sows but third litter sows had significantly higher titers than the first two groups. Antirotavirus IgG was high in colostrum but nearly nonexistent in milk. This titer did not vary significantly within or among parities. There was a linear regression in the titers of baby pig serum antirotavirus IgG from the post colostral sample through to seven weeks old, after which titer began to increase. No difference in baby pig serum antirotavirus IgG was noted among the three litters. Serum antirotavirus IgA and IgM were undetectable in baby pig sera after 2-3 weeks of age. Coproantibody to rotavirus was sporadically present in pig feces for 2-3 weeks after birth with highest titers in the IgA fraction. We conclude that although it is probable that age resistance of pigs to rotavirus diarrhea occurs, humoral immunity as measured by ELISA rotavirus antibody titers may not be intimately involved in virus clearance since in our studies baby pigs passively received large amounts of antibody but still excreted pathogenic virus. The finding of increasing levels of serum antirotavirus IgG in gilt/sow serum suggest that exposure to antigen of dams occur without significant increases in antirotavirus IgG titers in either colostrum, milk, or baby pig serum.     

Comparison of the virulence of two isolates of porcine parvovirus in 72-day-old porcine fetuses.

Two strains of porcine parvovirus (PPV), designated Kresse and NADL-8, were compared for relative virulence in porcine fetuses. Strain Kresse was injected into the amniotic fluid of all fetuses of 1 uterine horn of each of 2 pregnant gilts at 72 days of gestation. Strain NADL-8 was administered similarly to fetuses of 4 other gilts at the same stage of gestation. All gilts were killed and necropsied 35 days later. Selected tissues of all fetuses were tested for infectious virus and viral antigen. Sera from live fetuses were tested for antibody to PPV. These tests confirmed that most fetuses exposed to PPV by intra-amniotic injection became infected. All of 11 fetuses exposed to strain Kresse by intra-amniotic injection were alive at the time of necropsy, and all appeared clinically normal. In contrast, 8 of 24 fetuses exposed similarly to strain NADL-8 were dead. Many of the fetuses from the uterine horns contralateral to the uterine horns inoculated with virus were infected after 72 days of gestational age by intrauterine spread of the virus. Four such fetuses, 3 infected with the NADL-8 strain and 1 infected with the Kresse strain, were dead at the time of necropsy. These findings were inconsistent with those of a previous report, which indicated that the Kresse strain of PPV was markedly more virulent than the NADL-8 strain of PPV for porcine fetuses. A possible reason for this apparent discrepancy is discussed.     

Attempts to establish congenital bluetongue virus infections in calves.

Three bovine fetuses were inoculated in utero with approximately 10(3) plaque forming units of type 11 bluetongue virus. The gestational ages of the fetuses at the time of inoculation were 106, 113 and 122 days. They were spontaneously aborted 104, 65 and 109 days later, respectively, and the first and third of these fetuses were recovered. There was no grossly normal cerebral tissue, the meninges formed fluid filled sacs, and the cerebellums were reduced in size. Bluetongue virus was not isolated from the fetuses but the older one had neutralizing antibody. The three dams developed neutralizing antibody to bluetongue virus. The present work supports the observation by others that early fetal infections with bluetongue virus normally result in severe central nervous system damage and not in clinically normal, persistently infected calves.     

Experimental infection of 3-week-old conventional colostrum-fed pigs with porcine circovirus type 2 and porcine parvovirus

This report describes an experimental infection with porcine circovirus type 2 (PCV2) in combination with porcine parvovirus (PPV) in 3-week-old conventional colostrum-fed pigs with maternal antibodies to both viruses. Two groups of four pigs each were inoculated with PCV2 and PPV. One of the groups received also a commercial inactivated vaccine against porcine pleuropneumonia to evaluate possible effects of the stimulation of the immune system of pigs on the infection. Another group of four pigs was kept as uninfected control. Clinical signs, rectal temperatures and body weights were recorded. Serum antibody titers to PCV2 and PPV were determined at weekly intervals. Pigs were killed 42 days after inoculation and tissue samples were examined for the presence of gross and microscopic lesions. Tissues were also analyzed for the presence of PCV2 and PPV DNA by PCR, and for the presence of PCV2 antigen by immunohistochemistry (IHC). All the pigs had serum antibodies to PCV2 and PPV at the beginning of the trial. None of them developed clinical symptoms or pathological lesions typical of post-weaning multisystemic wasting syndrome (PMWS), a disease associated to PCV2 infection. However, IHC and/or PCR analyses showed that clinically silent PCV2 infection developed in five of the eight inoculated pigs, regardless of the administration of the vaccine. In particular, PCV2 DNA and/or antigen were detected in most of the tissues examined in the two pigs with the lowest titer of maternal PCV2 antibodies at the beginning of the trial. PPV DNA was not detected in any of the samples examined. The five pigs with PCR and/or IHC evidence of PCV2 infection had a mean weight gain during the experiment lower than that of the inoculated PCR-negative pigs considered together and that of the control pigs. In conclusion, it would appear that passive immunity against PCV2 can play a role in preventing the development of PMWS, but is not able to prevent the establishing of clinically silent PCV2 infections. The dissemination and persistence of the virus in the tissues may depend on the level of PCV2 antibodies at the time of inoculation.     

Evaluation of serology,bacteriological isolation and polymerase chain reaction for the detection of pigs carrying Actinobacillus pleuropneumoniae in the upper respiratory tract after experimental infection

Pigs, asymptomatically infected with Actinobacillus pleuropneumoniae in their upper respiratory tract, can transmit the infection. Detection of such animals is indispensable to prevent the intake of the disease in a herd. This study was conducted to evaluate bacteriology, polymerase chain reaction (PCR) and serology for the detection of subclinically infected pigs. Pigs were inoculated onto the tonsils with an A. pleuropneumoniae serotype 9 strain (n=12, group 1) or phosphate buffered saline solution (PBSS) (n=5, group 2). To prevent infection of the lungs, pigs of group 1 were treated three times with sodium ceftiofur as an aerosol. A third group (n=5) was inoculated intranasally with the same strain. All animals were euthanized 30 days post-inoculation (dpi). In pigs of group 1, clinical signs were not observed. A small lung lesion was found in only one pig and A. pleuropneumoniae was isolated from this lesion. The bacterium was not isolated from the lungs of animals that did not develop lung lesions. A. pleuropneumoniae was demonstrated in tonsils of 9/12 animals using bacteriological isolation, whereas it was demonstrated in mixed bacterial cultures from tonsils of all 12 animals by PCR. In non-infected animals (group 2), clinical signs were not observed and A. pleuropneumoniae was not demonstrated in any sample. All intranasally infected animals (group 3) developed disease signs and lung lesions. High antibody titers against ApxI, ApxII and heat-stable antigens were detected in animals that developed lung lesions. Antibody titers against these antigens were low or absent in all other pigs. It was concluded that pigs carrying A. pleuropneumoniae in the upper respiratory tract generally do not show measurable antibodies in serum. Therefore, sensitive methods for the detection of the etiological agent such as PCR are required to identify carrier animals, while serological methods are not suitable.     

Immune response of pigs inoculated with virulent pseudorabies virus and pigs inoculated with attenuated or inactivated pseudorabies virus vaccine before and after challenge exposure

Pseudorabies virus (PRV) antibodies, detectable by indirect radioimmunoassay (IRIA), serum-virus neutralization test (NT), or microimmunodiffusion test (MIDT) were developed within 8 days after pigs were inoculated with virulent PRV or attenuated PRV vaccine. Indirect radioimmunoassay and NT titers in pigs inoculated with virulent PRV were developed at the same rate, with IRIA titers being higher than NT titers. Pigs inoculated with attenuated or inactivated PRV vaccine developed peak mean prechallenge NT antibody titers of 4 and 1 (reciprocals of serum dilutions), respectively. Pigs inoculated with attenuated PRV vaccine had peak mean prechallenge IRIA antibody titers of 6, whereas pigs inoculated with inactivated PRV vaccine had mean IRIA antibody titers of 64. Challenge exposure of swine inoculated with attenuated or inactivated PRV vaccine elicited quantitatively equivalent responses, as measured by IRIA or NT, which were higher than prechallenge titers. There were no false-positive IRIA, NT, or MIDT results obtained when sera from nonvaccinated, nonchallenge-exposed pigs were tested. It appears that the PRV infection status of a seropositive swine herd could be ascertained by serologically monitoring several representative animals from a herd, using the NT. If 2 or more tests of representative animals at 14-day intervals were done and the mean NT titer was 4 or less, it could be concluded that the herd was vaccinated against, but not infected with, virulent virus.     

Acute and latent infection by bovine herpesvirus type 5 in experimentally infected goats

The ability of alphaherpesviruses to infect different ruminant species may have important implications for control/eradication efforts. Serological data indicate that goats may be naturally infected with bovine herpesviruses. To investigate the susceptibility of goats to bovine herpesvirus-5 (BoHV-5), 3-4-month-old kids were inoculated intranasally with each of three Brazilian BoHV-5 isolates (G1, n=8; G2, n=5; G3, n=5). The acute infection was characterized by virus shedding in nasal secretions for up to 14 days (titers up to 10(5.97)TCID(50)/mL), mild respiratory signs and conjunctivitis. All animals seroconverted to BoHV-5, developing virus neutralizing (VN) titers from 4 to 32 to the homologous viruses. At day 60 post inoculation (pi), two animals from each group were euthanized for tissue collection and the remaining goats were submitted to dexamethasone administration (0.4 mg kg(-1) for 5 days). Dexamethasone treatment resulted in virus reactivation in 9 out of 12 animals, as ascertained by virus shedding and/or by increase in VN titers. Virus shedding was detected in 8/12 animals and lasted from 1 to 9 days. Latent viral DNA was detected by PCR in the olfactory bulb and/or trigeminal ganglia of 6/6 goats euthanized at day 60 pi and in 12/12 animals euthanized 40 days post-dexamethasone. These results show that young goats are susceptible to BoHV-5 and may shed virus upon reactivation of latent infection. Thus, it is reasonable to expect that goats raised in close contact with cattle in areas where BoHV-5 is endemic may be infected and therefore should be considered potential reservoirs of the virus.     

Pigs orally inoculated with swine hepatitis E virus are able to infect contact sentinels

The purpose of the present study was to explore the most likely natural route of infection of swine hepatitis E virus (HEV) by oral inoculation of pigs and to investigate the potential infection by direct contact exposure. A preliminary experiment was performed to assess the infectiousness of the bile used as source of virus. Once confirmed, 16 pigs were inoculated via oral drop with an HEV positive bile suspension containing 2 × 10⁵ genome equivalents per pig. Nine animals were kept as contact sentinels and 12 more pigs were used as negative controls. A number of pigs from the three groups were euthanized at 16, 32 and 64 days post-inoculation. From the HEV inoculated group, three pigs shed virus in faeces, two had virus RNA in bile at necropsy and two seroconverted. In the contact group, two animals showed presence of HEV RNA in bile. This study demonstrates that pigs orally inoculated with a single HEV dose got infection, although few animals had evidence of infection. Moreover, the virus was successfully transmitted to direct contact exposed pigs.     

A COMPLEMENT-FIXATION TEST FOR ENZOOTIC PNEUMONIA OF PIGS USING A COMPLEMENT DILUTION METHOD

Complement-fixing antibody to Mycoplasma hyopneumoniae in the serums of pigs experimentally infected with enzootic pneumonia was demonstrated by comparing the haemolytic titre of guinea-pig complement titrated in the presence of heated test serum, M. hyopneumoniae antigen and unheated normal pig serum with the titre obtained when the antigen was omitted. The haemolytic titres against sensitised sheep erythrocytes were determined after a fixation period of 16 to 18 hours at 5°C. When serums, collected at intervals of 3 to 7 days, from 43 pigs exposed to pigs experimentally infected with enzootic pneumonia were tested, 4.6 or more complement units were first fixed 14 to 44 (mean 23.4) days after contact began. Serums collected subsequently fixed from 4.6 to more than 31 complement units. This positive reaction usually persisted until the pigs were killed 4 to 35 weeks after contact began. Thirty-three had gross enzootic pneumonia lesions and 9 had lung lesions detected microscopically. Serum antibody was not detected in 73 weaned pigs aged 7 weeks in a pneumonia-free herd but serums from 9 of 15 unweaned piglets aged 9 to 14 days in the same herd, fixed between 3 and 7 complement units.     

Antibody responses of guinea-pigs, rabbits and pigs to inactivated porcine parvovirus vaccines

Antibody responses were compared in guinea-pigs, rabbits and pigs following vaccination with inactivated porcine parvovirus (PPV) vaccines. Mean PPV hemagglutination inhibition (HI) antibody titers of 52, 56 and 36 at 1 week after first vaccination and 896, 640 and 512 at 2 weeks after second vaccination were detected in guinea-pigs, rabbits and pigs, respectively. PPV vaccines prepared with greater concentrations of virus, as determined by hemagglutination (HA) units, and of aluminum hydroxide gel adjuvant, induced higher HI antibody titers in guinea-pigs. Optimal concentrations for inducing consistently high antibody titers consisted of vaccine virus with a HA titer of 256/0.1 ml and gel adjuvant at a final concentration of 50%. A second vaccination at 4 weeks compared to 2 or 3 weeks after first vaccination resulted in higher mean HI titers. These data provide preliminary information on the use of guinea-pigs or rabbits as laboratory animal models for testing the potency of PPV vaccines.     

3种非猪瘟病毒单独或混合感染对猪瘟弱毒疫苗免疫效力的影响

将 2 0头 9月龄左右猪瘟、伪狂犬、猪繁殖与呼吸障碍综合征抗原、抗体阴性猪分成 6组 ,分别利用猪细小病毒(PPV)、猪伪狂犬病毒 (PRV)和猪繁殖与呼吸障碍综合征病毒 (PRRSV)单独或混合感染。 7d后连同对照猪 4头 ,免疫接种猪瘟兔化弱毒疫苗 (HCL V) ,13d后连同 4头阴性对照猪一起攻击猪瘟石门强毒。整个试验期间分别每天测温 ,观察临床症状 ,每周采集扁桃体和血样做各种病毒抗原及抗体检测。结果表明 ,非猪瘟病毒感染 7d后 ,所有各组猪均从体内检测到了相应感染的病原 ,表明 3种非猪瘟病毒感染成功。在攻击猪瘟石门强毒后 2周 ,感染了非猪瘟病毒后接种 HCL V疫苗的 4个免疫组 12头猪除 1头外 ,11头全为猪瘟病毒 (HCV)抗原检测阳性 ,且多呈强阳性 ;而单一 HCL V疫苗免疫组在猪瘟强毒攻击后检测不到 HCV;所有 HCL V疫苗免疫猪均存活 ,而非免疫对照组 4头猪全部在攻毒 16 d内死亡。     

Experimental production of congenital persistent swine fever infections: I. Clinical,pathological and virological observations

Twelve sows were inoculated with a low-virulent field strain of swine fever (SF) virus at 40, 65 and 90 days of pregnancy. Transplacental infection occurred in eight sows and these farrowed 88 piglets.Prenatal mortality was highest in litters from sows infected at 40 days after service, and postnatal death was most frequent in litters from sows infected at 65 days. Three sows gave birth to completely infected litters, whereas the five others farrowed litters in which uninfected piglets were found. The later the sows were infected during pregnancy, the more uninfected piglets were born. Twelve piglets recovered from the infection and the percentage of recoveries increased with the stage of pregnancy at which inoculation took place. Twenty-three piglets developed a persistent infection. The earlier infection occurred during pregnancy, the more persistent infections were produced. The persistently infected pigs developed a runting syndrome from about one week after weaning. The clinical signs were more severe in pigs from sows infected at 65 days of pregnancy than in pigs from sows infected at 40 days. A persistent viraemia was present in these pigs with titres ranging between 10^5.7 and 10^7.0 plaque forming units/ml of plasma. At autopsy the most pronounced lesions were an atrophy of the thymus, and swollen and pale lymph nodes. Virus antigen was present in lymphoidal, reticulo-endothelial and epithelial tissues.One persistently infected pig survived superinfection with a virulent strain of SF virus for 45 days.